Investigation of escape mechanisms by tumor cells from the immunological defenses of the host was continued. The hypothesis proposed for immunoresistance in the strain nonspecific TA3-Ha and TA3-MM mammary carcinoma ascites cells, namely, masking of histocompatibility (H-2a) antigens at the cell surface by large mucin-like glycoprotein molecules (epiglycanin), is supported by antibody absorption studies and physicochemical and morphological results. Recent transplantation experiments performed in both syngeneic (A/WySn) and allogeneic (C57BL) recipients show no immunosuppressive activity by epiglycanin and are consistent with the masking hypothesis. Injection of the glycoprotein under various conditions prior to challenge by TA3-Ha ascites cells had no detectable effect upon either the tumor growth rate or the time of death (due to tumor growth) of the animals. No antibody to epiglycanin was detected in mice after injection of epiglycanin (with Freund's complete adjuvant) alone, but antibody could be detected in both syngeneic and allogeneic mice 3 to 4 weeks following injection of TA3-Ha cells. In two other immunoresistant cell lines, TA3-St/ticol/-A mouse mammary carcinoma and YACIR mouse lymphoma, large cell-surface glycoproteins were also demonstrated. These were not detected in the corresponding immunosensitive lines, TA3-St and YAC, respectively. No evidence has been obtained to implicate these glycoproteins in an antigen-masking mechanism. (AG)